A typical human heart 10, depicted in cross sectional long axis view in FIG. 1, is a muscular organ that pumps deoxygenated blood through the lungs to oxygenate the blood and pumps the oxygenated blood to the rest of the body by rhythmic contractions of four chambers.
After having circulated in the body, deoxygenated blood from the body enters the right atrium 12 through the vena cava 14. Right atrium 12 contracts, pumping the blood through a tricuspid valve 16 into the right ventricle 18. Right ventricle 18 contracts, pumping the blood through the pulmonary valve 20 into the pulmonary artery 22 which divides into two branches, one for each lung. The blood is oxygenated while passing through the lungs and reenters the heart to the left atrium 24.
Left atrium 24 contracts, pumping the oxygenated blood through the mitral valve 26 into the left ventricle 28. Left ventricle 28 contracts, pumping the oxygenated blood through the aortic valve 30 into the aorta 32. From aorta 32, the oxygenated blood is distributed to the rest of the body.
Mitral valve 26, depicted in FIG. 2A (top view) and in FIG. 2B (cross sectional long axis view) is defined by an approximately circular mitral annulus 34 that defines a mitral valve orifice 36. Attached to the periphery of mitral annulus 34 is an anterior leaflet 38 and a smaller posterior leaflet 40, leaflets 38 and 40 joined at commissures 41.
The typical area of mitral valve orifice 36 in a healthy adult is between 4 and 6 cm2 while the typical total surface area of leaflets 38 and 40 is approximately 12 cm2. Consequently and as depicted in FIG. 2B, during ventricular systole leaflets 38 and 40 curve downwards into left ventricle 28 and coapt to accommodate the excess leaflet surface area, producing a coaptation surface 42 that constitutes a seal. The typical depth of coaptation surface 42 in a healthy heart 10 of an adult is approximately 7-8 mm.
Anterior leaflet 38 and posterior leaflet 40 are connected to papillary muscles 44 of left ventricle 28 by chordae 46.
During atrial systole, left atrium 24 contracts to pump blood into left ventricle 28 through mitral valve 26. The blood flows through mitral valve orifice 36, pushing leaflets 38 and 40 into left ventricle 28 with little resistance.
During ventricular systole, left ventricle 28 contracts to pump blood into aorta 32 through aortic valve 30. Mitral annulus 34 contracts pushing leaflets 38 and 40 inwards and downwards, reducing the area of mitral valve orifice 36 by about 20% to 30% and increasing the depth of coaptation surface 42. The pressure of blood in left ventricle 28 pushes against the ventricular surfaces of leaflets 38 and 40, tightly pressing leaflets 38 and 40 together at coaptation surface 42 so that a tight leak-proof seal is formed. To prevent prolapse of leaflets 38 and 40 into left atrium 24, papillary muscles 44 contract, pulling the edges and body of leaflets 38 and 40 into left ventricle 28 through chordae 46.
An effective seal of mitral valve 26 is dependent on a sufficient degree of coaptation, in terms of depth, area and continuity of coaptation surface 42. If coaptation surface 42 is insufficient or non-existent, there is mitral valve insufficiency, that is, regurgitation of blood from left ventricle 28 into left atrium 24. Mitral valve insufficiency leads to many complications including arrhythmia, atrial fibrillation, cardiac palpitations, chest pain, congestive heart failure, fainting, fatigue, low cardiac output, orthopnea, paroxysmal nocturnal dyspnea, pulmonary edema, shortness of breath, and sudden death.
There are a number of pathologies that lead to a mitral valve insufficiency including collagen vascular disease, ischemic mitral regurgitation, myxomatous degeneration of leaflets 38 and 40 and rheumatic heart disease as well as physical anomalies that allow leaflet prolapse (e.g., elongated or ruptured chordae 46, weak papillary muscles 44) or prevent coaptation (e.g., short chordae 46, small leaflets 38 and 40).
In ischemic mitral regurgitation (resulting, e.g., from myocardial ischemia or infarction), and other myocardial disease (e.g. Dilated cardiomyopathy) leaflets 38 and 40 and chordae 46 have normal structure and the mitral valve insufficiency results from altered geometry of left ventricle 28. As a result of ischemia, portions of the heart walls necrose. During healing, the necrotic tissue is replaced with disorganized tissue leading to remodeling of the heart which reduces coaptation through distortion/dilation of mitral annulus 34 and outwards sagging of the outer wall of left ventricle 28 which displaces papillary muscles 44.
In FIGS. 3A (top view) and 3B (cross sectional long axis view), the reduction of coaptation and incomplete closure of a mitral valve 26 during ventricular systole resulting from ischemia is depicted for an ischemic heart 50 that has undergone remodeling and suffers from ischemic mitral regurgitation. In FIG. 3B is shown how a wall of left ventricle 28 sags outwards, distorting mitral annulus 34 and displacing papillary muscles 44 outwards which, through chordae 46, pulls leaflets 38 and 40 apart and into left ventricle 28, reducing coaptation.
Initially, ischemic mitral regurgitation is a minor problem, typically leading only to shortness of breath during physical exercise due to the fact that a small fraction of blood pumped by left ventricle 28 is pumped into left atrium 24 and not through aortic valve 30, reducing heart capacity. To compensate for the reduced capacity, left ventricle 28 contracts harder and remodeling continues. Ultimately leaflet coaptation is nonexistent as leaflets 38 and 40 are pulled further and further apart, leading to more blood regurgitation, further increasing the load on left ventricle 28, and further remodeling. Ultimately, the left side of the heart fails.
Apart from humans, mammals that suffer from mitral valve insufficiency include horses, cats, dogs, cows, sheep and pigs.
U.S. Pat. Nos. 3,656,185, 6,183,512 and 6,250,308 and United States Patent applications published as US 2002/065554, US 2003/0033009, US 2004/0138745 or US 2005/0038509 describe ways of treating mitral dysfunction.
U.S. Pat. No. 6,332,893 describes valve to myocardium tension members.
It has been proposed to change the shape of a left ventricle 28 and/or to support the walls of a left ventricle 28 to improve the functioning of a mitral valve 26, see for example, the U.S. Patent Application published as US 2006/0281968, U.S. Pat. No. 7,238,152 (as well as products of Paracor Medical, Inc., Sunnyvale, Calif., USA) and U.S. Pat. Nos. 6,077,214, 6,332,893 and 6,723,038 (as well as products of Myocor, Inc., Maple Grove, Minn., USA such as Coapsys®).
In “RING plus STRING”: Papillary muscle repositioning as an adjunctive repair technique for ischemic mitral regurgitation” by Langer, F and Schafers, H-J in J Thorac Cardiovasc Surg 2007; 133; 247-249 is taught implantation of an undersized annuloplasty ring together with deployment of a suture passing through the left ventricle 28 from the head of the posterior papillary muscle 44 to the midseptal fibrous annulus through the aortic wall underneath the commissures of two aortic valve 30 leaflets. While the heart beats and under observation of an imaging device, the suture is tensioned so as to pull the papillary muscle 44 towards the aortic wall until a desired degree of mitral valve leaflet coaptation is observed. The method leads to an increased tension applied to papillary muscle 44, which may stretch and elongate, affecting the angle at which papillary muscle 44 pulls leaflet 38.